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10.0:
Headache associated with metabolic disorder
There
are a variety of types of headache that may be associated with different
derangements of metabolism. This subject is only covered briefly in this
chapter and the interested reader is referred to other more extensive
headache texts such as Dalessio (1993) and Raskin (1988).
10.1:
Hypoxia
Headache
Associated with Hypoxia
Dalessio
(1993) points out that experimentally induced cerebral hypoxemia, (Wolff
and Lennox, 1930), especially when coupled with an increase in carbon
dioxide tension in the blood, results in extreme dilatation of cerebral
vessels, notably of the arteries and arterioles. This observation is
probably related to the fact that some persons at high altitudes
(Bancroft et al., 1922; Monge, 1942) complain of headache that persists
for hours or days until physiologic adjustments have been achieved, or
until the individual returns to a lower altitude. Such headaches are
usually prevented by ingestion of acetazolamide prior to ascent to high
altitude. Associated with the intense throbbing headache is a sensation
of fullness of the head, hot flushes of the face, photophobia, injection
of the ocular mucosa, and deep cyanosis. It is likely that such
headaches are due to cerebrovascular distention.
There
are a variety of specific situations in which headache may occur from
hypoxia alone or from hypoxia and hypercapnia together, as described
below.
Decompression
Headache
Arterial
hypoxia, not contaminated by hypercapnia, occurs in those exposed to
high altitudes and in those in decompression chambers. Decompression
sickness appears when a sudden change in the pressure of ambient gases,
to which the subject has become equilibrated, occurs. A sudden reduction
in pressure of 45% is usually sufficient to cause symptoms.
The
symptoms produced by rapid decompression are caused primarily by the
formation of nitrogen gas bubbles in blood and fatty tissues. Nitrogen
does not diffuse readily and is not used in body metabolism. When body
fluids and tissues saturated with nitrogen are suddenly exposed to a
lower pressure, bubbles of nitrogen gas form that lodge in small blood
vessels and fatty tissues, because nitrogen is five times more soluble
in oil than in water (Behnke, 1965).
Most
decompression sickness now occurs in sports divers (Dalessio, 1993). The
neurologic complications can be striking (Erde and Edmonds, 1975; Kidd
and Elliott, 1975). Both the spinal cord and brain are affected.
Bilateral throbbing headache occurs frequently and at times may be the
only symptom of decompression sickness. The headache can be
indistinguishable from migraine without aura. A migraine attack after
decompression may require recompression therapy, as the headache itself
is indistinguishable from that produced by arterial gas embolism to the
brain.
Treatments
for both high-altitude and decompression sickness are generally
preventive. Descent from altitude will abolish some manifestations but
may only retard others. Thus, aviators who have experienced
decompression sickness should not be re-exposed even to low altitudes of
flight for 72 to 96 hours, since re-expansion of nitrogen bubbles
already present in fatty tissues may exacerbate their signs and symptoms
(Dalessio, 1993).
Adequate
recompression therapy is the only specific treatment for decompression
sickness. At times this may require prolonged recompression, for more
than several days. All other measures can be considered as ancillary,
including the use of 100% oxygen and methods to retard or prevent brain
edema (dexamethasone, 8 to 10 mg every 4 to 6 hours, and intravenous
injection of mannitol or dextran).
Headache
Associated with High Altitude
Theses
headache occur within 24 hours after sudden assent to altitudes above
3000 meters and, according to IHS coding criteria, are associated with
at least one or other symptoms typical of high altitude, namely: Cheyne
Stokes respirations at night, desire to overbreath, and dyspnea.
Appenzeller
(1972) pointed out that headache may be associated with acute mountain
sickness, acute pulmonary edema of altitude, and chronic mountain
sickness in well-acclimatized subjects. Altitude headache is uncommon
below 8,000 feet, appears with increasing frequency at higher
elevations, and above 12,0000 feet is more or less universal in persons
not acclimatized to altitude.
10.2:
Hypercapnia
Retention
of CO2 causes vasodilatation and diffuse headache.
Chronic hypercapnia from pulmonary disease and situations such as the
Pickwickian syndrome are often accompanied by increased intracranial
pressure and severe diffuse headache similar to that seen in pseudotumor
cerebri. The diagnostic criteria are that there is an arterial pCO2
increased above 50 mm Hg in the absence of hypoxia.
10.3:
Mixed hypoxia and hypercapnia
This
type of headache is often seen in pulmonary patients such as those
alluded to below in which there is a combination of hypoxia and
hypercapnia as in the Pickwickian syndrome. In this syndrome, obese
person usually with accompanying pulmonary disease, develop chronic
hypoxia and hypercapnia. Papilledema and severe headache are often
accompaniments.
10.4:
Hypoglycemia
Headaches
may be precipitated by attacks of hunger and by fasting. Precipitation
of migraine by hunger (Blau and Cummings, 1966) led to several studies
of carbohydrate metabolism. Although headache is a common symptom of
insulin-induced hypoglycemia (Hockaday, 1975), it clearly is not
hypoglycemia per se that is responsible for the precipitation of
migrainous attacks by hunger (Pearce, 1971). The lowest blood glucose
levels recorded during fasting in subjects experiencing an attack are
not different from those in subjects who do not develop headache (Hockaday
et al, 1971).
During
extended standard insulin hypoglycemia tests, migrainous subjects
demonstrate hypoglycemia unresponsiveness (Rao and Pearce, 1971). Since
the cortisol response to insulin-induced hypoglycemia and the metapyrone
test is normal in migraineurs, a defect of the
hypothalamic-pituitary-adrenal axis is not likely to be contributory. A
diminished hyperglycemic response to glucagon (DeSilva et al, 1974) is
consistent with an impairment in the hepatic mobilization of glucose.
During migraine attacks, decreased glucose tolerance, low plasma insulin
levels, an elevations of free fatty acids (Anthony, 1986), glycerol,
ketone bodies, secretin (McLoughlin et al, 1978), and growth hormone
(Shaw et al, 1977) are noted. These findings (Table 36.2) taken
together, are consistent with a chronic stress reaction with heightened
sympathetic activity (Taggart et al, 1973). Fasting results in increased
turnover of brain serotonin (Curzon et al, 1972), which may be important
to the mechanism of headache provoked by hunger.
10.5:
Dialysis
Headache
occurs with varying degrees of severity during dialysis in about 70
percent of dialyzed patients (Raskin, 1988). The most common form of
"dialysis headache" is the precipitation of migraine headaches
in those with preexisting migraine. Other patients without previous
headache disorders experience headache only in association with
dialysis, usually during the third or fourth hour. It is usually
reported as bilateral and throbbing without focal neurologic symptoms (Bana
et al, 1972). Headaches may disappear after nephrectomy or after a
successful transplant. Later, if the transplant is subsequently
rejected, headaches may reappear as a symptom of rejection continuing
until nephrectomy is carried out (Graham, 1976). There is some evidence
that arterial renin and 18-hydroxy-11-deoxycorticosterone levels,
obtained during hemodialysis, are lower in patients who are subject to
headache (Graham, 1976; Bana et al, 1972; Bana and Graham, 1978).
However, the preponderance of evidence points to shifts of water into
the brain as the major cause of "disequilibrium," the term
denoting a conglomeration of symptoms, including headache, that occur
during or after dialysis (Arieff et al, 1978).
Quoting
from Raskin (1988), "The mechanism of these symptoms was originally
believed to be the lag in the reduction of brain urea compared to blood
urea because of the influence of the blood-brain barrier. This effect
was thought to produce an osmotic gradient between blood and brain,
resulting in movement of water into brain, leading to cerebral edema,
increased intracranial pressure, and symptoms of encephalopathy. This
hypothesis became known as the reverse urea effect; the unequal effects
of dialysis upon tissue and blood solutes, resulting in an osmotic
gradient, underlies the naming of this disorder the disequilibrium
syndrome. Experimental models of disequilibrium support the hypothesis
that osmotically active substances are ("idiogenic osmoles")
are present in brain in the dialyzed uremic animal (and not in the
dialyzed nonuremic animal), creating an osmotic gradient between brain
and blood that results in shifts of water into brain (Raskin and
Fishman, 1976). The nature of the idiogenic osmoles is not clear, but
they must play a role because the amount of urea transiently retained in
the brain is not sufficient to account for cerebral edema, nor are
alterations in brain or plasma sodium likely to underlie disequilibrium.
The marked lowering in cerebrospinal fluid (CSF) pH that occurs in
dialyzed uremic animals may reflect the cerebral accumulation of organic
acids, and such osmotically active solutes may also be important to the
genesis of the neurologic disturbances that occur associated with
hemodialysis."
10.6:
Headache related to other metabolic abnormality
Adrenal
Dysfunction
Raskin
(1988) reported a patient with lifelong migraine who had worsening of
her headache attacks concurrent with involvement of Conn’s syndrome.
Following subtotal adrenalectomy her migraine attacks ceased (Stanford
and Greene, 1970). Similarly, Cushing’s syndrome and the hypoadrenal
state following steroid withdrawal may be the source of de novo
headaches that resemble migraine (Graham, 1976). Headache is a complaint
of over 40 percent of patients with Cushing’s syndrome (Ross and Linch,
1982). The secretion of many pituitary-derived hormones, including ACTH,
is influenced by central serotonergic mechanisms, as is aldosterone
secretion (Shenker et al, 1985).
According
to Glueck and Bates (1986), migraine occurs with higher than chance
frequency among patients with hyperlipidemias and dyslipoproteinemias.
Restoration of serum lipids to normal levels with clofibrate
dramatically improved the headache problem in a well-studied patient (Leviton
and Camenga, 1969). However, the treatment of dyslipoproteinemias in
large populations of patients does not appear to reduce the frequency
and severity of headaches (Leviton, 1986). Whether the alteration in
serum viscosity that accompanies hyperlipidemia is important to the
trigger mechanism of headache is not clear.
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